Alzheimer's disease (“AD”) is believed to be a multifactorial degenerative disease rather than the result of a single malfunction or agent. Although AD is usually accompanied by the abnormal accumulation of extracellular deposits or plaques of β-amyloid protein (AB) and intracellular neurofibrillary tangles of tau protein (NFTs), extensive research has not isolated or identified a cause for the accumulation, nor shown that β-amyloid protein or NFTs are the cause rather than effect of AD. In fact, approximately 30 percent of AD patients have no AB plaques or NFTs at death, and approximately 30 percent of cognitively normal adults do have AB plaques and NFTs at death. AB plaques may even be protective against harmful soluble AB oligomers. Instead, clinical and epidemiological studies have identified numerous contributing factors to AD.
Many of the pathologic characteristics of AD, inflammation, oxidative stress, impaired cerebral blood flow and glucose utilization, result from body imbalances, including stress, obesity, and an overloaded immune system. In addition, AD has a lengthy, non-linear, accelerating, and degenerative prodromal time period with ample opportunity for preventive intervention, and about 95 percent of AD cases are sporadic late-onset.
However, no comprehensively-effective medicine or protocol has emerged for AD or other dementias. Yet it is estimated that about 44 million patients suffer from AD or a related dementia worldwide. Cognitive decline affects significantly more. New compositions designed on the growing understanding of neurobiochemistry, cognitive decline, AD, other dementias, and neurodegeneration in general are needed.